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1
Departments of Medicine and Immunology, Mayo Clinic, Rochester, MN 55905
Aging and chronic inflammatory syndromes, such as rheumatoid
arthritis, are associated with high frequencies of
CD4+CD28null T cells, which are rarely seen in
healthy individuals younger than 40 years. Inasmuch as rheumatoid
arthritis and aging are also associated with elevated levels of
TNF-
, we examined whether this proinflammatory cytokine influences
CD28 expression. Incubation of T cell lines and clones as well as
Jurkat cells with TNF- induced a reduction in the levels of cell
surface expression of CD28. This effect of TNF- was reversible;
however, continuous culture of CD4+CD28+ T cell
clones in TNF- resulted in the appearance of a CD28null
subset. In reporter gene bioassays, TNF- was found to inhibit the
activity of the CD28 minimal promoter. Inactivation of the promoter was
accompanied by a marked reduction in DNA-protein complex formation by
two DNA sequence motifs corresponding to the transcriptional initiator
of the CD28 gene. Indeed, in vitro transcription assays showed that
nuclear extracts from TNF--treated cells failed to activate
transcription of DNA templates under the control of a consensus TATA
box and the CD28 initiator sequences. In contrast, similar extracts
from unstimulated T cells supported transcription. These results
demonstrate that TNF- directly influences CD28 gene transcription.
We propose that the emergence of CD4+CD28null T
cells in vivo is facilitated by increased production of
TNF-.
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